Placodes

Placodes are neuroectodermal thickenings that form outside of the boundaries of the CNS and contribute to the paired specialized sense organs (olfactory/nose, optic/lens, otic or auditory/ear, and lateral line system) or to the anterior pituitary gland and cranial sensory ganglia (Fig. 16). Many early marker genes have been identified that are expressed in specific placodes such as Pax6, Otx2, and Sox3 in the lens placodes, Pax6 in the olfactory placodes; Nkx5.1 Pax8, and Pax2 in the otic placodes; Msx2 and Dlx3 in the lateral line placodes; Pax3, FREK, and neuro-genin1 in the trigeminal placodes; and Pax2 and neurogenin2 in the epibranchial placodes that form the principal ganglia of the Vllth, IXth, and Xth cranial nerves (see Baker et al, 1999 and references therein). However, how these regional specifications are patterned is still a work in progress (reviewed extensively by Baker and Bronner-Fraser, 2001).

In brief, a region of ectoderm competent to form the cranial placodes, the preplacodal domain, forms in the cranial neural plate border region. The expression of several Pax (paired-box transcription factor) genes in this ectoderm such that each placo-dal region expresses a different combination of Pax expression (see above). In Drosophila, Pax homologs (Ey and Toy) function synergistically with other transcription factors (so) and transcription factor facilitators (eya and dac). Various members of the vertebrate homologs of these transcription regulators, (Six, Eya, and Dach) are expressed with the various Pax genes in the placodes, suggesting that a conserved network of genetic regulation may be responsible for establishing specific placodal identity/pattern.

These transcription factors are regulated by signals from various sources. For olfactory placodes the anterior endoderm, prechordal mesoderm, and the anterior neural ridge all have been suggested as sources of inducing signal responsible for activating the appropriate set of transcription factors, although no signal has yet been identified that is either sufficient or necessary for olfactory placode induction. The hypophyseal placode is originally specified by BMP4 from the diencephalon. For lens placode induction, exposure to neural plate and anterior mesendoderm are sufficient, whereas exposure to the optic cup is both necessary and sufficient (via BMP4 and 7). For the trigeminal placodes, an interaction between the neural tube and the surface ectoderm is required to induce the placode but the signal and the method of restricting the placode to a certain location have not been determined. For the lateral line placode, neural plate, axial, and nonaxial mesoderm are each sufficient for induction, and no signaling molecule has been identified. For otic placode formation, evidence points to mesendoderm as the source for an early signal, and to hindbrain as the source for a later signal in a two-step model of early ear patterning. For the epibranchial placodes, pha-ryngeal pouch endoderm expressing BMP7 is both necessary and sufficient. In summary, placodes are dependent on local environmental signals from various sources to initiate specific sets of highly conserved transcription regulators, which define their fate in the AP plane.